Health & Evidence Library
Guides to diabetes, metabolic risk, complications, screening, research interpretation, and practical prevention across the life course.
89 guides · Page 1 of 2
SURMOUNT-5 head-to-head data on tirzepatide (Zepbound) versus semaglutide (Wegovy) for weight loss: how much each works, side effects, and choosing.
Over-the-counter CGMs are marketed to healthy people, but the evidence for benefit is thin. Here is what glucose data does and does not tell you.
Twin studies show strong genetic liability for diabetes while discordant identical twins prove that genes do not determine one person's outcome.
Mendelian randomization uses genetic variants as instruments for causal questions. Its conclusions depend on relevance, independence, exclusion, and design.
Informed consent is an ongoing, voluntary communication process in clinical research, not a signature. Learn its elements, safeguards, and limits.
Heritability describes variation in a population under particular conditions; it does not measure genetic destiny, immutability, or an individual's risk.
GWAS identify statistical links between genomic regions and traits. Learn how they work, why association is not causation, and what scores inherit.
Learn how FDA evaluates biosimilar insulin through analytical similarity, potency, PK and PD studies, immunogenicity, manufacturing quality, and labeling.
Routine vitamin D blood testing in asymptomatic adults has unproven benefit. Learn what 25-hydroxyvitamin D measures and when targeted testing differs.
Basal insulin covers background needs between meals, while bolus insulin addresses food and high glucose; safe use depends on patterns and timing.
Type 2 diabetes remission has a specific definition. Learn how it is measured, how it may occur, why relapse happens, and what follow-up remains necessary.
Treat-to-target insulin trials seek the same glucose goal, making hypoglycemia, dose, weight, safety, and usability central comparisons.
TI-RADS scores ultrasound features and biopsy thresholds. Bethesda classifies sampled cells. Learn how the two systems guide one thyroid nodule pathway.
The thrifty gene hypothesis links past food scarcity with modern metabolic disease, but its selection story and genetic predictions remain unsettled.
Pancreatic islets coordinate insulin, glucagon, somatostatin, blood flow, nerves, and nutrient signals to stabilize metabolism between meals.
Pharmacokinetics tracks drug concentration over time; pharmacodynamics links concentration to effects. Learn ADME, half-life, clearance, response, and dosing.
Insulin resistance means tissues respond less effectively to insulin. Learn how the body compensates, what tests can show, and why context matters.
Understand GLP-1 receptor agonists and dual GIP/GLP-1 therapy, including uses, outcomes, side effects, dose escalation, and safety.
Learn why diabetic ketoacidosis develops, how euglycemic DKA can occur, which warning signs matter, and why hospital treatment is urgent.
Compare insulin, metformin, SGLT2 inhibitors, GLP-1-based therapy, sulfonylureas, DPP-4 inhibitors, and other diabetes medicines.
Diabetes burnout and distress can make daily care feel impossible. Learn how to recognize overload, reduce burden, and find appropriate support.
What the U.S. screening recommendation at age 35 actually covers, why the threshold changed, and how abnormal results are confirmed.
How adipose tissue stores and releases fuel, sends hormonal signals, supports immunity and temperature control, and changes with location.
How safety reports become signals, how active surveillance tests them, and why one report cannot establish that a medicine caused an event.
Moving from phase 2 to phase 3 fixes far more than a trial number. It selects the dose, population, endpoints, comparator, and evidence strategy.
A neutral map of the medical-manager function across evidence strategy, trial design, safety interpretation, governance, and regional coordination.
A euglycemic clamp maps basal insulin action under controlled conditions, but it cannot by itself prove better glucose outcomes or fewer low-glucose events.
A clinical study report links one trial's protocol, conduct, analyses, efficacy, safety, and participant-level support in a reviewable record.
Connect renal and hepatic function, drug disposition, study design, unbound concentrations, modeling, clinical response, and labeling decisions.
How the liver stores, makes, and releases glucose across meals, fasting, exercise, diabetes, and liver disease.
Why oral glucose produces a larger insulin response than matched intravenous glucose, what GIP and GLP-1 do, and how type 2 diabetes changes the physiology.
Gut microbes and their metabolites are linked with diabetes, but medicines, diet, geography, and disease itself complicate cause and effect.
Diabetes genetics moved from families and candidate genes to GWAS, sequencing, fine-mapping, diverse cohorts, and functional studies of beta cells.
Morning glucose can rise before breakfast because circadian signals increase liver glucose output. Learn how to identify the pattern and its mimics.
Pancreatic alpha cells do more than oppose insulin. Learn how glucagon coordinates liver glucose, amino acids, fasting, exercise, and hypoglycemia.
Testosterone results vary with timing, illness, SHBG, assay method, and reference range. Learn why repeat morning testing and clinical context matter.
Mildly high TSH with normal free T4 is common and can be transient. Treatment decisions depend on persistence, age, context, symptoms, and evidence.
How ICH E8(R1) defines fitness for purpose, identifies critical-to-quality factors, and uses proportionate risk controls across a trial.
How FDA Project Optimus reframed cancer-drug dose selection around benefit, tolerability, pharmacology, and randomized dose comparisons.
How calcium and PTH establish primary hyperparathyroidism, what mimics it, and why urine, kidney, and bone findings complete the assessment.
Why primary aldosteronism is often missed, how aldosterone and renin screening works, what affects the ratio, and how confirmation and subtype guide care.
A rigorous comparison of family linkage, genetic association, recombination, linkage disequilibrium, causal inference, and study limitations.
How laboratory studies, clinical trials, and PBPK models turn an interaction mechanism into a practical label recommendation.
A plain-language guide to dose selection, concentration-response evidence, dose-ranging trials, labeling, and reasons a dose may need review.
What a DSUR contains, how it connects cumulative safety evidence to action, and why annual reporting does not replace urgent reporting.
Follow a diabetes GWAS signal through fine-mapping, cell-specific regulation, target-gene evidence, perturbation, and functional confirmation.
How researchers separate genetic susceptibility, environmental factors, joint effects, and true interaction in type 2 diabetes studies.
How noncoding variants, enhancers, chromatin maps, and functional studies help researchers interpret the genetics of type 2 diabetes.
How laboratory studies separate circadian phase, sleep-wake timing, and meals when testing glucose regulation, plus the limits of the evidence.
Nocturnal hypoglycemia results depend on glucose thresholds, nighttime windows, measurement methods, episode rules, and observation-time denominators.
How a 2022 endocrine working group replaced 'diabetes insipidus' with etiology-based names, and what the patient safety evidence behind the change shows.
How incretin hormones like GLP-1 signal after eating to shape insulin release, stomach emptying, and appetite, explained in plain language.
How type 2 diabetes genetics actually work, from polygenic risk and beta-cell biology to what a DNA report can and cannot tell you.
A polygenic risk score for type 2 diabetes sorts groups by inherited risk but cannot predict any one person, and ancestry changes how accurate it is.
How inherited gene differences change a drug's effect, with real promise for a few medicines and honest limits for most of them.
A plain explainer on monogenic diabetes and MODY, the rare single-gene forms that are often mistaken for type 1 or type 2.
How type 2 diabetes runs in families, why it is not simple inheritance, and what a family history does and does not predict.
How insulin works inside a cell, from the receptor to IRS proteins to the PI3K and AKT relay to GLUT4, and where insulin resistance breaks the chain.
How the pancreatic beta cell senses glucose and releases insulin, why failing secretion drives type 2 diabetes, and what that means for treatment.
A high glucose reading can come from tissues ignoring insulin or from a pancreas that cannot make enough, and the two need different care.